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Finals > REB Renal > Flashcards

REB Renal Flashcards

1
Q

what part of the nephron is involved in converting vitamin D to active form

A

PCT

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2
Q

what organ produces erythropoietin

A

kidney

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3
Q

what is the renal capsule

A

tuft of capillaries and bowman’s capsule

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4
Q

where does ultrafiltration take place

A

glomerulus

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5
Q

ultrafiltration is dependant on

A

string hydrostatic pressure in the nephron

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6
Q

approximately how much filtrate is formed everyday?

A

180L

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7
Q

how much filtrate is excreted in urine?

A

1.5L

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8
Q

how much filtrate is reabsorbed?

A

178.5L

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9
Q

how much water, glucose and salt is reabsorbed (%)?

A

water - 99
glucose - 100
salt - 99.5

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10
Q 
Reabsorption of which of the following are active and which are passive
water 
glucose 
amino acids 
na
cl
A

passive
cl
water

active
glucose
amino acids
na

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11
Q

What is the passage of substances which are are reabsorbed in the kidney?

A

Lumen to cells to ECF

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12
Q

What is the passage of tubular secretions?

A

Peritubular capillaries to tubular lumen

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13
Q

What’s molecules are involved in tubular secretion and what is the importance of this process?

A

H+, K+, organic ions, wastes

Important for removal of waste and maintaining blood pH by secreting H+ and NH4+

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14
Q

How much urine is formed per min?

A

1 ml/min

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15
Q

What is the typical pH of urine?

A

Six

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16
Q

What does substances are commonly found in urine?

A 
Water
urea
creatinine
ions
phenol
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17
Q

Outline the blood supply to the glomerulus

A

Renal - interlobular - arcuate - interlobular - afferent

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18
Q

What is a normal BP range? (MAP)

A

MAP - 80-180 mmHg

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19
Q

How is the afferent arteriole affected by changes in arterial pressure?
Why is this important?

A

Changes in arterial pressure or matched by a corresponding change and afferent arteriole resistance
This maintains a constant flow rate

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20
Q

What are the types of intrinsic regulation of renal blood flow?

A

myogenic

Tubuloglomerular feedback

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21
Q

What is myogenic regulation of renal blood flow?

A

Stretch of walls of afferent arteriole followed by reflexed contraction of smooth muscle which increases pressure and stretch –> activates nonselective cation channels in smooth muscles –> Ca2+ depolarises

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22
Q

In myogenic regulation of renal blood flow, what cation channels are activated and cause depolarisation?

A

Calcium

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23
Q

Where are macula densa cells found?

A

At the junction between the ascending loop of Henle and the distal convoluted tubule

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24
Q

Macular densa sells changes tone in response to

A

Changes in the rate of blood flow

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25
Q

When there is an increased glomerular filtration rate, there is an increase in the delivery of which ions to the macula densa?

A

Sodium and chloride

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26
Q

What paracrine agents does the macula densa release?

A

ATP and adenosine (to increase GFR)

NO ( to decrease GFR)

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27
Q

How do macula densa cells increase tone?

A

increased pressure –> increased glomerular filtration rate –> increased Na+/Cl- delivery to macula densa –> activates non-selective cation channels –> macula densa to releases paracrine agents such as ATP and adenosine –> increases the tone of afferent arterioles

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28
Q

How do you glomerular capillaries maintain GFR

A

They are fragile

COOL!

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29
Q

Can GFR be extrinsically controlled?

A

No

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30
Q

explain extrinsic control of renal blood flow?

A

1.nerves - sympathetic fibres
noradrenaline –> constriction –> decreases GFR
2.hormones - the vascular smooth muscle cells are sensitive to adrenaline and angiotensin II

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31
Q

the release of what neurotransmitter decreases GFR

A

noradrenaline

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32
Q

how is renal blood flow controlled at rest?

A

autoregulation only

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33
Q

how is renal blood flow controlled during severe exercise?

A

sympathetic NS
adrenaline
–> cause constriction

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34
Q

how is renal blood flow controlled if there is a hemorrhage?

A

heavy SNS activity
adrenaline
–> reduces fluid loss in urine

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35
Q

how is renal blood flow controlled if there is a long hemorrhage?

A

NO2 and prostaglandins (PGE2, PGI2) released by macula densa cells

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36
Q

what is the effect of a long-term hemorrahage?

A

renal ischemia –> hypoxia –> tubular necrosis

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37
Q

how much plasma entering the nephron is filtered in bowman’s capsule

A

20%

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38
Q

what factors influence glomerular filtration (3) and give their values

A
  1. glomerular capillary pressure - 55mm Hg
  2. plasma colloid osmotic pressure - 30 mmHg
  3. bowman’s capsule hydrostatic pressure - 15 mmHG
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39
Q

what is the net filtration pressure?

A

10 mmHg

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40
Q

Creatinine come from _____ which is stored in _____ and synthesised from _____ in the ______ for quick bursts of energy.
Creatinine is formed spontaneously by ______ at a constant rate of ___% and its level depends on _____.
It composes ___% of the nitrogenous component of urine

A

creatine
skeletal muscles
arginine
liver

phosphocreatine
2%
muscle mass

4%

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41
Q

what conditions change GFR

A
  1. alterations in the forces:
    - decrease in plasma protein –> increases GFR
    - urinary tract blockage –> decreases GFR and increases pressure in bowman’s capsule
    - diarrhea –> increased plasma colloid –> decreased GFR
  2. autoregulation and extrinsic control
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42
Q

how does a decrease in plasma protein affect GFR

A

increases GFR

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43
Q

how does a urinary tract blockage affect GFR and p in the BC

A

decreases GFR and increases pressure in bowman’s capsule

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44
Q

how does diarrhea affect GFR

A

increased plasma colloid –> decreased GFR

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45
Q

compare the value of osmolarity in the renal corpuscle and in plasma

A

same - 300 mosm/L

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46
Q

what is the pH of the filtrate in the renal corpuscle

A

6

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47
Q

what part of the nephron has cuboidal epithelial cells?

A

PCT

thick limb LoH

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48
Q

what part of nephron has microvilli?

A

PCT

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49
Q

what part of nephron has squamous epithelium

A

thin LoH

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50
Q

what part of nephron has a lot of mitochondria?

A

PCT

thick limb LoH

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51
Q

function of microvilli

A

increase reabsorption

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52
Q

what does water move through in the nephron?

A

tight junctions

aquaporins

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53
Q

the PCT and thin descending limb have what type of aquaporin?

A

1

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54
Q

the DCT and collecting tubules have what type of aquaporin?

A

2 (3,4)

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55
Q

what aquaporins are mediated by ADH?

A

2 (3,4)

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56
Q

are all aquaporins bidirectional?

A

yup!

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57
Q

are the Na/K pumps located on the basal or apical membrane?

A

basal

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58
Q

the apical membrane borders the _____ whilst the basal membrane borders the ____

A

lumen

ECF

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59
Q 
what % of the following is reabsorbed in the PCT 
glucose 
aa
HCO3-
phosphate 
Na
K
H2O
urea
lactate
A

100%
glucose
aa

HCO3- 90%

phosphate - 85%

70%
Na
K
H2O

50%
urea
lactate

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60
Q

where does NaCl reabsorption occur

A

early PCT

late PCT

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61
Q

what transporters are involved in the reabsorption of NaCl?

A

early PCT
Na/organic solute cotransporter
Na/H exchanger
**impermeable to CL-

Late PCT
only Na/H exchanger

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62
Q

where is this transporter found:

Na/organic solute cotransporter

A

early PCT

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63
Q

where is this transporter found:

Na/H exchanger

A

early PCT

Late PCT

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64
Q

the early PCT is impermeable to

A

Cl-

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65
Q

how Cl get through the late PCT?

A

passively diffuses through paracellular pathway

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66
Q

where does glucose reabsorption occur

A

early PCT

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67
Q

what transporters are involved in the reabsorption of glucose?

A 
SGLT2 cotransporter (na and glucose in)
exit through GLUT 2 (1 way)
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68
Q

which transporter is a target for diabetic medications to lower glucose level?

A

SGLT2 cotransporter

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69
Q

all glucose is reabsorbed until maximum (Tmg) of

A

2 mmol/min

** 3 times the normal amount

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70
Q

where does protein reabsorption occur?

A

**only some enters filtrate

PCT

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71
Q

how is protein reabsorbed in the PCT?

A

through receptor-mediated endocytosis where they are digested by lysosomes into AA

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72
Q

where does AA reabsorption occur?

A

**either directly from glomerular filtration through digestion of protein by lysosomes or through peritubular blood

early PCT but if there is a lot in the filtrate, it can occur throughout PCT

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73
Q

what transporters are involved in the reabsorption of AA?

A

Na/aa cotransporter

they exit through different separate passive channels on basal membrane

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74
Q

can HCO3- cross the apical membrane?

A

NOPE

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75
Q

explain the reabsorption of HCO3-

A

HCO3- combines with H+ (which are secreted by Na/H exchangers) to produce H2CO3 which is then broken down into H2O and CO2 by carbonic anhydrase
CO2 and H2O enter passively and then recombine to form HCO3- and H+
HCO3- leaves through the HCO3/Na symporter (basal)

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76
Q

what reaction is catalysed by carbonic anhydrase

A

H2CO3 –> H2O and CO2

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77
Q

explain organic ion secretion in the PCT include the transporters

A

secretion –> body –> lumen
this the main method for transporting wastes and drugs

this occurs through MDR1 (multidrug) or Na/K-dependant transport

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78
Q

HCO3- leaves through the

A

HCO3/Na symporter (basal)

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79
Q

what is Fanconi syndrome

A

disease of PCT dysfunction

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80
Q

Fanconi syndrome is characterised by

A

excess loss of glucose, aa, phosphate, HCO3- into urine

this leads to acidosis and dehydration

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81
Q

Fanconi syndrome is treated by

A

hydration and supplements

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82
Q

what the 3 divisions of the LOH

A

Thin descending
thin ascending
thick ascending

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83
Q

what is the main function of the LoH

A

maintenance of the highly concentrated medulla and reabsorption of water

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84
Q

osmolarity varies from ____ to ___ in the LoH to _____ in the DCT

A

300 mosm/L
1200
100

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85
Q

the thin descending LoH has a low permeability to _____ but high permeability to _____

A

solutes

water

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86
Q

what happens to [filtrate] as water is reabsorbed in the LoH

A

the filtrate becomes more concentrated

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87
Q

the thin ascending LoH has a impermeable to _____ but permeable to _____

A

water

solutes

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88
Q

what happens to [filtrate] as NaCl is reabsorbed in the thin ascending LoH

A

the filtrate becomes less concentrated

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89
Q

what is reabsorbed in the thin ascending LoH

A

NaCl

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90
Q

the thick ascending LoH actively reabsorbs what ions

A

na
k
cl

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91
Q

what transporters are involved in the reabsorption of ions in the thick ascending LoH

A

NKCC2

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92
Q

how do the reabsorbed ions from the thick ascending LoH exit the nephron

A

cl and k through basolateral transporters
na through the Na/K pump
some K leaks back into the cell through the apical membrane

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93
Q

what is the effect of K+ leaking into the lumen

A

positive lumen –> cation absorption via tight junction

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94
Q

how do loop diuretics work

A

inhibiting the NKCC2 transporter in the thick ascending LoH which inhibits salt reabsorption and increases water excretion

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95
Q

what patients use loop diuretics

A

suffer from renal insufficiency or severe edema

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96
Q

in the early DCT, Na+ enters the apical membrane through

A

Na/Cl transporters

or NCC

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97
Q

the early DCT reabsorbs ____ but not ____.

how does it affect [filtrate]?

A

NaCl
water
filtrate is dilute

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98
Q

what hormone acts at the DCT to cause calcium reabsorption

A

parathyroid hormone

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99
Q

explain calcium reabsorption in the early DCT (include transporter)

A

enters apical site through facilitated diffusion and exits through the 3Na/Ca exchanger at the basolateral membrane

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100
Q

what are the 2 types of epithelial cells in the late DCT and the CD? what do they control?

A

principal cell - NaCl transport

intercalated cells - acid/base balance

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101
Q

in principal cells, Na+ is reabsorbed through ___ channels and _____

A

NCC

ENaC (electrogenic)

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102
Q

ENaC is under the control of

A

aldosterone

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103
Q

what regulates the concentration of urine based on body’s needs?

A

combined effect of ADH and Aldosterone

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104
Q

ENaC transports ___ ions into the cell from the lumen, leaving a _______ charge where the ___ ion exits

A

na
negative
k

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105
Q

there is a dramatic increase in ___ ion secretion in the late DCT and CD

A

K

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106
Q

K+-sparing diuretics target

A

ENaC

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107
Q

ADH or vasopressin regulates what aquaporin? where is this aquaporin located?

A

2

DCT and CD

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108
Q

other than the opening of aquaporins, ADH also regulates

A

urea absorption

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109
Q

what is the importance of urea absorption regulation by ADH

A

to maintain hypertonic medulla

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110
Q

ADH is released in response to

A

thirst

low Bp

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111
Q

in the intercalated cells, H+ is excreted across the apical membrane into the tubular fluid wia what transporters?

A

H+ATPase pump
or
H+/K+ ATPase exchangers

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112
Q

H+ secretions in the DCT and CD affect urinary pH to a minimum of

A

4.5

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113
Q

how much filtrate enters the CD on average

A

12 ml/min

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114
Q

discuss the changes to urine production when the is no ADH, average ADH and high ADH

A

no - 12 ml/min (o ml reabsorbed)
average - 2 ml/min (10 ml reabsorbed)
high - 0.5 ml/min (11.5 ml reabsorbed)

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115
Q

___% of the filtrate left with variable NaCl and H2O reabsorption at DCT and CD

A

10

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116
Q

__% of nephrons are juxtamedullary nephrons

A

15

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117
Q

salt pumps in the thick ascending limb maintains the ____mosm/L difference between the filtrate and surrounding interstitium

A

200

118
Q

what is the anatomical arrangement of vessels so that one vessel is in the opposite direction of adjacent vessels?

A

countercurrent exchanger system

119
Q

what is the anatomical arrangement of the LoH so that it concentrates solutes in renal medulla?

A

countercurrent multiplier

120
Q

what is the main driving force of the countercurrent mechanism

A

active salt pump in thick ascending limb transports NaCl actively out of lumen and into interstitium until the interstitium is 200 mosm/L more conc than filtrate

121
Q

which parts of the nephron are completely impermeable to urea

A

LoH

DCT

122
Q

does urea concentration increase or decrease in the LoH and DCT

A

increases

123
Q

how does ADH affect the reabsorption of urea. (include RECEPTORS)

A

ADH acts on collecting ducts to increase permeability of urea by promoting UTA1 and UTA3.

124
Q

explain the recycling of urea.

A

some urea excreted goes to the medulla to increase concentration while some diffuses back into the LoH to be recycled

125
Q

how much urea ends up in urine? (%)

A

20%

126
Q

why isn’t the hypertonic interstitium washed away?

A
  1. blood flow to medulla is very low
  2. vasa recta capillaries operate as countercurrent exchange flow (equilibrates the medulla so net change is 0) –> goes up to 300 mosm/L
127
Q

fluid movement from the ICF to the IF is _______ pressure

A

osmotic

128
Q

fluid movement from IF to plasma is _____ pressure

A

hydrostatic

129
Q

what is the function of RAAS

A

to control volume and blood pressure

130
Q

what would happen if RAAS is not present

what condition is RAAS particularly important in

A

ischemia due to lower oxygen perfusion

hemorrhage

131
Q

what is the rate limiting step of the RAAS

A

fall in Bp causes renin (produced by kidneys) to convert angiotensinogen (from liver) into angiotensin I. it cleaves at the leu-val bond.

132
Q

what triggers the release of renin

A

fall in Bp

133
Q

where is renin produced

A

juxtaglomerular cells in the kidney

134
Q

what bond does renin cleave

A

leu - val

135
Q

where is angiotensinogen produced?

A

liver

136
Q

where is ACE located?

A

endothelial cells of the lung

137
Q

what is the action of ACE

A

activated ang I by converting it to ang II (main effector)

138
Q

what bond is cleaved by ACE

A

his - leu

139
Q

what is renin first produced as

A

pre prorenin

140
Q

where is renin stored

A

secretory granules until release when Bp is low

141
Q

where are juxtaglomerular cells found

what type of cells are they

A

juxtaglomerular apparatus formed by DCT and glomerular afferent arteriole
specialised smooth muscle

142
Q

the position of juxtaglomerular cells at the glomerular afferent arteriole allows it to sense

A

Bp and GFR

143
Q

what do the macula densa cells sense

A

NaCl absorption

144
Q

how do the macula densa cells and the juxtaglomerular cells communicate

A

macula densa secretions of PHE2 and PGI1

145
Q

what receptor is involved when factors induce renin release (and 2nd messenger)

A

GsPCR and camp

146
Q

what receptor is involved when factors inhibit renin release (and 2nd messenger)

A

GqPCR and Ca2+

147
Q

use of ACE and renin inhibitors

A

used for patients with high Bp to decrease it

148
Q

a decrease in Bp in the afferent arteriole is sensed by

A

baroreceptors on the juxtaglomerular cells

149
Q

what factors induce renin secretion

A
  1. decrease in Bp in the afferent arteriole
  2. decreased NaCl reabsorption
  3. increase in adrenergic activity by sympathetic stimulation via B-adrenergic receptors and arteriole constriction via alpha adrenoreceptors
150
Q

An increase in adrenergic activity by sympathetic stimulation via _____ receptors and arteriole constriction via _____ induces renin release.

A

B-adrenergic

alpha adrenoreceptors

151
Q

what factors inhibit renin secretion

A
  1. increased NaCl reabsorption
  2. increased afferent arteriole Bp
  3. decreased adrenergic activity / sympathetic stimulation
  4. Ang II by negative feedback
152
Q

what are the ang II receptors?

A

AT1R

AT2R

153
Q

AT1R primarily mediates

A

cardiovascular effects of ANd II

154
Q

what are AT1R receptors located

A

AT1Ra - blood vessels

AT1Rb - adrenal cortex and ant pit

155
Q

what type of receptor is AT1R

A

GPCR linked to Phospholipase C with Ca+ as its second messenger as well as cAMP

156
Q

use of AT1R inhibitors

A

treat hypertension and heart failure

157
Q

where are AT2R located

A

fetus

neonate

158
Q

function of the AT1R (5)

A
  1. tubular Na+ reabsorption in PCT by stimulating Na/H exchanger, Na/K ATPase and NA/HCO3- cotransporter
  2. vasoconstriction
  3. aldosterone release
  4. ADH release
  5. negative feedback to renin release in juxtaglomerular cells
159
Q

tubular Na+ reabsorption in PCT is done by stimulating

A

Na/H exchanger
Na/K ATPase
NA/HCO3- cotransporter

160
Q

what is the function of aldosterone

A

enhanced reabsorption of Na+ in the DCT –> water follows and K+ is excreted

161
Q

aldosterone increases the expression of

A

ENaC

Na/K ATPase

162
Q

effects of hyperaldosteronism

A

hypertension and hypokalemia
adenoma (gland - primary)
decreased renal perfusion (not in gland - secondary)

163
Q

effects of hypoaldosteronism

A

hypotension and dehydration
addison’s (primary)
decreased renin production (SECONDARY)

164
Q

what receptors are acted on by ATP

A

aquaporin 2

UTA 1 and 3

165
Q

GFR is the main diagnostic tool to determine

A

renal fxn (index of renal fxn)

166
Q

renal clearance is the

A

ml of plasma cleared of a substance in 1 min or Cs in ml/min

167
Q

renal clearance is involved in measuring

A

the rate of excretion of a substance in relation to its plasma concentration

168
Q

equation for Cs

A

(Us x V)/Ps

169
Q

a decrease in GFR is a clinical sign of

A

renal disease

170
Q

what is the criteria for substances that can be used to find clearance

A

must enter filtrate through filtration only

flows through the nephron and exits urine without being absorbed

171
Q

relationship between inulin excretion and its plasma concentration

A

inulin excretion proportional to its plasma concentration

172
Q

how does the plasma concentration of inulin affect the amount of inulin filtered

A

as plasma conc rises, more inulin is filtered in and ready to be excreted

173
Q

the slope between rate of excretion and plasma conc represents the

A

clearance of inulin

174
Q

is clearance dependent or independent of plasma conc?why?

A

independent

as plasma conc of inulin increases, clearance remains the same

175
Q

how is inulin administered?

A

through IV

176
Q

is inulin produced in the body?

A

NOPE

177
Q

other than inulin, what substance can be used to find clearance

A

creatinine

178
Q

what is creatinine

A

waste product of muscle cell’s creatine

179
Q

is creatinine accurate to calculate clearance? explain.

A

not totally
a small quantity of creatinine is secreted into the tubule from paratubular vessels (affecting Us) but is approximately cancelled out by error in estimation of plasma concentration of creatinine (affecting Ps) which also detects another compound

180
Q

Cin = Ccr =

A

125ml/min

181
Q

formula for Ccr in males

A

Ccr = [(140-age) x weight (kg)] / [72 x Pcr (mg/dL)]

182
Q

how does age, gender and weight affect Ccr

A

increased age - decreased Ccr
increased weight - increased
male - increased

183
Q

formula for Ccr in females

A

[(140-age) x weight (kg)] / [72 x Pcr (mg/dL)] x 0.85

184
Q

if someone is an athlete, how is their Ccr affected

A

increased

185
Q

if someone if lean, how is their Ccr affected

A

decreased

186
Q

freely filtered, not absorbed, not secreted
renal clearance =
give an example

A

GFR

inulin, creatinine - 125ml/min

187
Q

freely filtered, fully reabsorbed, not secreted
renal clearance =
give an example

A

0ml/min

glucose and aa

188
Q

freely filtered slightly reabsorbed, not secreted
renal clearance is
give an example

A

less than GFR

urea - 65 ml/min

189
Q

freely filtered, not reabsorbed, fully secreted
renal clearance =
give an example

A

renal plasma flow

PAH - 625 ml/min

190
Q

PAH asses and indicates ____ to the kidneys

A

blood supply

191
Q

renal failure is a reduction in ____ so that kidneys cannot maintain their salt/water balance nor excrete waste

A

GFR

192
Q

describe the onset of acute renal failure

A

fast onset

reversible or fatal

193
Q

what type of renal failure is characterised by:
abrupt and rapid decline in renal fxn with a rapid onset caused by altered blood supply, toxins or urinary tract abnormalities

A

acute

194
Q

edema is a consequence of what type of renal failure

A

acute

** salt and water retention

195
Q

hyperkalemia is a consequence of what type of renal failure

A

acute

196
Q

cardiac arrhythmias is a consequence of what type of renal failure

A

acute

197
Q

hyperphosphatemia is a consequence of what type of renal failure

A

acute

198
Q

Itching due to waste-product retention is a consequence of what type of renal failure

A

acute

199
Q

what are the types of renal failure

A

acute
subacute
chronic

200
Q

is chronic renal failure reversible?

A

NOPE

201
Q

what type of renal failure is characterised by:

gradual irreversible loss of large numbers of functioning nephrons

A

chronic

202
Q

in chronic renal failure, the electrolyte fluid balance is maintained at ____% of renal failure

A

20-30

203
Q

chronic renal failure can go symptomatic until __% of the nephron is lost and is fatal after ___%

A

70

90

204
Q

treatment of chronic renal failure

A

dialysis

205
Q

what is the relationship of clearance of creatinine and plasma concentration of urea

A

inversely proportional

** used in estimating disease

206
Q

how does a decrease of creatinine affect plasma conc of urea

A

increases

207
Q

nitrogen is absorbed in our bodies from proteins in the form of ____ following fixation from bacteria in the gut

A

NH3

208
Q

nitrogen is formed in the body by the ____ of proteins and nucleotides

A

catabolism

209
Q

___g of nitrogen is brought in the body each day

A

16

210
Q

this nitrogen is formed into urea in the _____ and excreted in the kidney

A

liver

211
Q

nitrogen turnover is normally balanced where intake =

A

excretion

212
Q

a positive nitrogen balance indicates ____

where intake is ____ than excretion

A

growth/ pregnancy

greater

213
Q

a negative nitrogen balance indicates a catabolic state where excretion is ____ than intake

A

greater

214
Q

does protein synthesis increase or decrease nitrogen in the body

A

increase

215
Q

does protein catabolism increase or decrease nitrogen in the body

A

decrease

216
Q

nitrogen turnover is dependant on the ____ turnover

A

aa

217
Q

how much N is excreted as urea, as NH4+ and as uric acid/ creatinine (%)

A

85%
5%
10%

218
Q

Creatine is synthesised by what amino acid in the liver?

A

arginine

219
Q

Creatinine is formed at a constant rate of

A

2%

220
Q

uric acid is the end product of _____ metabolism and is freely filtered in the glomerulus

A

purine

221
Q

hyperuricemia is caused by

A

too much uric acid

222
Q

ammonia is made from metabolism of

A

glutamate

223
Q

urine is sterile and clear with ___% water and a pH of

A

93-97%

6

224
Q

what does each colour of urine indicate
dark
bright yellow
red

A

more conc
vit D / meds
blood (disease)

225
Q

what does the clarity or cloudiness of urine indicate
normal
abnormal

A

mucus, sperm, prostatic fluid

blood cells, bacteria

226
Q

a _____ (medical test) with colour identifying degree is used in the chemical analysis of urine

A

dipstick

227
Q

the presence of crystals in urine indicates

A

kidney stones

228
Q

the presence of epithelial cell is urine indicates

A

infection/ cancer

229
Q

the presence of hyaline in urine indicates

A

RBC
WBC
fat

230
Q

average pH of blood

A

7.35(v) - 7.45(a)

231
Q

factors that affect ph of urine (3)

A
  1. metabolism releases acid in the form of CO2
  2. breakdown of food –> nonvolatile acids (sulphuric and phosphoric)
  3. metabolic intermediates –> lactic acid –> non volatile
232
Q

nitrogenous components of urine and the amount of each (%) present in urine

A 
creatinine - 4%
uric acid - 1%
ammonia - 3%
urea - 40%
water and nacl
233
Q

can non-volatile/non-carbonic acids be removed by the lungs?

A

NOPE

234
Q

non-volatile/non-carbonic acids CANNOT be removed by the lungs. how are they removed and how much is removed per day.

A

bicarbonate buffer system by using HCO3-

1 mmol/day/kg

235
Q

blood pH is maintained by what organs

A

lung and kidney

236
Q

how does the lung maintain blood pH

A

respiratory regulation releasing Co2 as fast as it is produced

237
Q

how does the kidney maintain blood pH

A

HCO3- (base) control to buffer acid

238
Q

what are the 2 determinants of blood pH

A

H2CO3 (weak acid)

HCO3- (weak base)

239
Q

how is blood pH calculated given the concentration of the 2 determinants of blood pH

A

[HCO3-] / [H2CO3]

240
Q

[H2CO3] = pCO2 x ___

what does this number represent

A

0.03 - solubility of Co2 in the plasma

241
Q

[HCO3-] is maintained at __mmol/L

A

24

242
Q

pCO2 is maintained at ___mmHg

A

40

243
Q

pka of H2CO3 =

A

6.1

244
Q

pH of blood can be found by the equation

A

pka (H2CO3) + log [HCO3-] / [H2CO3]

where [H2CO3] = pCO2 x 0.03

245
Q

for every 1 mmol of HCO3- of non volatile acid that enters the blood, how much HCO3- is removed?

A

1 mmol

246
Q

when [H+] increases beyond the capacity of the buffer system, [HCO3-] ______ and hence HCO3- must be restored by the kidney.

A

decreases

247
Q

where does reabsorption of HCO3- occur

A

80% in the PCT

20% in the DCT and LoH

248
Q

describe how HCO3- is reabsorbed from filtrate

A
  1. H+ released from Na/H+ exchanger and binds to HCO3-
  2. H2CO3 becomes Co2 and H2O which enters the cell
  3. carbonic anhydrase reforms HCO3- and H+
249
Q

tubular cells breakdown H2O into

A

H+ and OH-

250
Q

H+ is secreted to the lumen through the _______ transporter and binds with ________ acids (HPO42-)

A

H+ATPase

non-volatile

251
Q

H+ is secreted to the lumen through the _______ transporter in the CD or ____ transporter in the PCT/DCT/CD and binds with ________ acids (HPO42-)

A

H+ATPase
Na/H+ exchanger
non-volatile

252
Q

HCO3- IS RELEASED INTO THE BLOOD THROUGH _____ CAPILLARIES

A

peritubular

253
Q

H+ is secreted more when the pH is ___

A

low

254
Q

titratable acid (33%) - H+ is buffered with filtrate buffers such as…. (2)

A
  1. phosphates (H2PO4- from HPO42-)

2. Creatinine (25%) in the DCT

255
Q

acid with ammonia (67%) - the _____ is the main site of NH4+ synthesis and hence it is also the main site for ______ –> NH4+

A

PCT

H+ + NH3

256
Q

pH above ____ is alkalotic

A

7.45

257
Q

pH below ____ is acidic

A

7.35

258
Q

which is faster: respiratory or renal adaptation

A

resp

259
Q

does an increase in pC02 increase or decrease ventilation?
what effect does it have on the kidney?
what effect does it have on H+?

A

increases
kidney produces HCO3- (renal compensation)
there is also increased H+ secretion

260
Q

does a decrease in HCO3-increase or decrease ventilation?

what effect does it have on the reabsorption of the HCO3-?

A 
increases vent (body changes HCO3- into CO2) (respiratory compensation)
increases reabsorption
261
Q

primary defect of respiratory acidosis

A

increased pCO2

262
Q

primary defect of meatbolic acidosis

A

decreased plasma HCO3- (under 24) due to an increase in other acids (other than H2CO3+)

263
Q

uncontrolled diabetes, lactic acidosis, severe diarrhea and renal failure are causes of _______ acidosis

A

metabolic

264
Q

how does insulin affect the pH (diabetic ketoacidosis)

A

inadequate insulin production –> decreased glucose use –> more FA metabolization and B oxidation –> ketone bodies are low in pH

265
Q

how does hyperglycemia affect nerve excitability and cardiac contractility

A

insulin regulates K+ entry into the cell. hyperglycemia –> decreased aldosterone –> concentration K+ and salty urine –> K+ leaks out of cell and cannot re enter without insulin –> hyperkalemia –> decreases nerve excitability and increased cardiac contractility

266
Q

primary defect of respiratory alkalosis

A

decreased pCO2

267
Q

primary defect of metabolic alkalosis

A

increased [HCO3-]

268
Q

explain the role of vomiting in metabolic alkalosis

A

causes H+ LOSS –> [HCO3-] remains elevated in plasma
**parietal cells secrete H+ into the lumen and HCO3- into the blood in anticipation of the reabsorption of H+ back into the blood
vomiting does not allow this to occur and hence the increase in [HCO3-] without reabsorption of H+ causes alkalosis

269
Q

parietal cells secrete __ into the lumen and ____ into the blood in anticipation of the reabsorption of ___ back into the blood

A

H+
HCO3-
H+

270
Q

how is the anion gap calculated

A

[unmeasured anions] = [Na+] - [Cl-] - [HCO3-] = anion gap

271
Q

describe the difference between metabolic acidosis with a high anion gap and with a normal anion gap

include examples of illnesses

A

high - unknown anions such as lactic acid and ketone bodies reduce [HCO3-] such as in diabetes

low - such as in diarrhea, loss of HCO3-
in the kidney there is an increase in CL- due to metabolic acidosis and the anion gap shifts back to normal although acidosis is maintained

272
Q

urinary epithelium is ______ epithelium

A

transitional

273
Q

what is the ureterorenal reflex

A

blockage of ureter causes a build up of urine and back flow to the kidney
sympathetic innervation causes the decrease in urinary output of the kidney

274
Q

what is the vesicoureteric reflux

A

issue with passage of ureter into the bladder causing the absence of the physiological valve –> contraction of detrusor muscle causes backflow to kidney

275
Q

what are the 3 layers of muscle in the bladder

A

inner circular
outer longitudinal
detrusor

276
Q

what characteristics of the bladder wall allow for increased volume in bladder without increasing pressure

A

transitional epithelium
rugae (folds in the walls)
smooth muscle plasticity

277
Q

when holding in urine, what nerve is being fired?

A

pudendal nerve (SOMATIC)

278
Q

the somatic innervation of the bladder is responsible for:

a. voiding
b. holding in urine

A

b

279
Q

the parasympathetic innervation of the bladder is responsible for:

a. voiding
b. holding in urine

A

a

280
Q

sympathetic innervation of the bladder is done by what nerve?

A

hypogastric (T10-L4)

281
Q

parasympathetic innervation of the bladder is done by what nerve?

A

pelvic nerve (S2-S4)

282
Q

somatic innervation of the bladder is done by what nerve?

A

S2-S4

283
Q

what NT is released by hypogastric nerve, what receptors do they act on and what is the result

A

Noradrenaline
on B3 receptor –> inhibits detrusor muscle
on alpha 1 receptor –> stimulation of internal sphincter

284
Q

what NT is released by pelvic nerve, what receptors do they act on and what is the result

A

ACH on M3 –> stimulates detrusor muscle

NO on M3 –> inhibits internal sphincter

285
Q

what NT is released by pudendal nerve, what receptors do they act on and what is the result

A

ACH acts on nicotinic receptor and acts on the external sphincter

286
Q

what part of the brain receives signals from the stretch receptors of the bladder?

A

pontine storage center

287
Q

high nerve firing indicates fullness and initiates the ______ maneuver (forced expiration) due to stimulation from the _______ in the brain

A

pontine micturition centre

288
Q

what are the 2 phases of spinal cord injury and loss of voluntary control

A
  1. areflexic - urinary retention **early

2. hyperreflexic - neurogenic detrusor overactivity **after a few weeks

289
Q

describe the areflexic stage

A

no sensation of full bladder –> accumulation of urine –> reflux –> damage to kidney

290
Q

describe the hyperreflexic stage

A

automatic bladder - patient has no control over the bladder or urination
the micturition reflex returns but is activated without conscious control –> overactivity of detrusor muscle

291
Q

hyperreflexic stage is due to overactivity of the _____ muscle

A

detrusor

Finals (17 decks)

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